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Molecular epigenetics (excerpted from Diamond, Binstock, and Kohl, 1996)"Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes.... Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans.... That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes."

The neuroscience of adaptive evolution

“With the help of a tiny worm, Cornelia Bargmann is unpicking the neural circuits that drive eating, socializing and sex.”

by Stephen S. Hall20 February 2013

Excerpt: “…these deaf, part-blind, transparent creatures, which resemble nothing so much as wriggling specks of lint, could nonetheless yield enormous insight into how a nervous system creates behaviour.”

My comment:

James Vaughn Kohl said:

Adaptive evolution appears to be nutrient-dependent and pheromone-controlled in species from microbes to man. This was demonstrated by Bumbarger et al (2013) in the context of: “System-wide Rewiring Underlies Behavioral Differences in Predatory and Bacterial-Feeding Nematodes.” Their approach incorporates aspects of ecological, social, and neurogenic niche construction elucidated by Cori Bargmann et al throughout her career, and in the honeybee model organism throughout the careers of many others. The three stages of niche construction are required to link sensory input to de novo protein synthesis (to genes) and to neurogenetically programmed behavior that enables social selection (for nutrient-dependent pheromone production).

Pheromones control genetically predisposed species-specific behavioral development via the control of nutrient-dependent reproduction in asexual and sexual variants of all species. The theme involves the epigenetic tweaking of immense gene networks by nutrients with control of the “tweaking” by pheromones, presumably via adaptive changes in the microRNA/messenger RNA balance.

Can we expect that a change in the diet of C. elegans would result in epigenetic tweaking manifested in the neurocircuitry of their sexual selection? If so, the results would go a long way towards explaining how an alanine substitution appears to alter the thermodynamics of intranuclear interactions, protein biosynthesis, and the adaptive evolution of nutrient-dependent physical traits associated with immune system function and with glandular secretions trapped by hair that contribute to pheromone production and distribution in a human population — as recently reported by Kamberov et al (2013) Modeling Recent Human Evolution in Mice by Expression of a Selected EDAR Variant and in Grossman et al (2013) Identifying Recent Adaptations in Large-Scale Genomic Data.

-------------------Some people think I am biased by my commercial interests-------------------

See also: Lucrative Prize for Life Scientists:Excerpt: This year’s recipients, who are free to use the money as they please, include Cornelia Bargmann, who investigates neural circuits and animal behavior at Rockefeller University…”

Nutrient-dependent “tweaking” of immense gene networks (revisited)

Excerpt: “…understanding our diets as a collection of signaling molecules, having hormone-like actions via cell-surface and nuclear receptor signaling, may provide new insights into the relationship between what we eat and metabolic disease.”

My comment:

I detailed the epigenetic effects of food odors associated with nutrient-dependent pheromone-controlled species diversity in Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338. My conclusion was based on the concept of the epigenetic “tweaking” of immense gene networks and extension of the honeybee model organism of cause and effect. Simply put, “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans.”

The clarity that Ryan and Seely add to the complex systems biology of adaptive evolution can now be addressed by further examination of other recent works. On Feb 14, 2013 two published papers in “Cell” focus on data that they use to eloquently elucidate virtually all of what is currently known about natural selection for nutrient-dependent adaptively evolved pheromone-controlled sexual selection in a human population. Taken together, Kamberov et al, and Grossman et al., have extended a mammalian model to humans in which a change in a single base pair results in an amino acid substitution with downstream effects on the thermodynamic regulation of organism-level survival.

The change is manifested in increased eccrine and apocine gland density and hair thickness that enables sexual selection for species-specific pheromone production via the actions of microbes on the glandular secretion of nutrient metabolites associated with sexually dimorphic visually appealing physical characteristics. This occurs in the same context as our development of food preferences, which is driven by chemical appeal, not by visual appeal.

Everything I know about animal models places nutrient-dependent pheromone-controlled adaptive evolution at the forefront of cause and effect, with effects on hormones that affect behavior. However, the link to nutrient-dependent disease processes is clearer in Ryan and Seely. I think they have made it more likely that people will compare what’s adaptive and maladaptive in terms of hormone-organized and hormone-activated evolved behavior via ecological, social, neurogenic, and socio-cognitive niche construction in vertebrates and invertebrates. Can we expect that the nutrient-dependent pheromone-controlled development of our socio-cognitive niche will enable us — like the honeybee — to make the best choices for our survival? If not, may God help us all.

I now refer to H. Allen Orr's review of Mind and Cosmos: Why the Materialist Neo-Darwinian Conception of Nature Is Almost Certainly False by Thomas Nagel.

"Awaiting a New Darwin"

There's no need to wait any longer. The epigenetic effects of nutrient chemicals and pheromones are on immense gene networks. For example, the epigenetic effect of one nutrient causes the formation of a receptor that lets it enter the cell. When it enters the cell it alters the thermodynamics of intracellular signaling and intermolecular interactions between the mitochondrial tRNA and its nuclear-encoded tRNA synthetase. That allows the epigenetic landscape to become the physical landscape of the cell's DNA. What happens next is that histone-driven chromatin remodeling and de novo protein biosynthesis occur. Nutrient-dependent de novo protein biosynthesis is required for stochastic gene expression and pheromone-controlled adaptive evolution.

Recent reports link the thermodynamics of antibiotic resistance in bacteria to sexually dimorphic traits that can be selected in a human population. The traits are associated with organism-level thermoregulation in the bacteria and in humans. That means I can again link nutrient-dependent pheromone-controlled adaptive evolution across species from microbes to man, sans mutations theory. This time, there is proof of the link from physics to biology (e.g., in the "RNA world" mentioned in Orr's review).

Arguments can now proceed in the context of whether or not the 2nd law of thermodynamics has been invalidated by a single base pair change that results in substitution of one amino acid for another. This occurs within the closed system of the cell. It results in organism-level changes in thermoregulation.

Since I'm not a physicist, I cannot predict the outcome of those arguments, except from what I know about biology. Physicists may simply state that the cell is not a closed system because nutrients enter. They may say that's why the reduction in entropy via de novo protein biosynthesis does not invalidate the 2nd law. Biologists may redefine mutations to make it appear as if they can cause adaptive evolution. I don't think they can get away with that, since a recent report on G-protein coupled receptors distinguishes between natural variants and disease-causing mutations. Evolutionary theorists may continue to say anything they like.

Nevertheless, whatever the argument is from physics or from biology, it is not likely to result in support for a mutation-driven model of adaptive evolution because there is no model for that. There never has been. I doubt that there will be. Even the population geneticists have realized that what's known about molecular epigenetics has forced them to think in terms of what's being selected. And, as we've seen in the pigeon study results, it's not the visual appeal of the head crest or other associated physical features -- except in theory. The truth hasn't changed, however. Natural selection occurs for nutrients and social selection is enabled by the metabolism of nutrients to species-specific pheromones. Sexual selection is a subset of social selection in many organisms.

takes decades of work, ignores my model, and arrives at the conclusion that: "Our understanding of epigenetic regulation of GnRH neurons and neuroendocrine function in general is in its infancy, though the three reports detailed in this review indicate the importance of a shifting epigenetic structure at genes responsible for the development of reproductive function. Presently, DNA methylation and histone modifications both appear to influence levels of GnRH gene expression through neuronal maturation."